The mechanism of monocyte-mediated killing is poorly understood. We have been investigating the mechanism of killing through various biochemical pathways. While SOD and catalase inhibit killing, direct measurement of superoxide production shows that both killer cells and fresh cells which do not kill produce equal amounts of superoxide. Likewise prostaglandin biosynthesis has no effect on killer function. Since S-adenosyl-L-methionine methylation is important in monocyte functions, we will investigate the effects of inhibiting methylation with competitive inhibitors. In addition, the lipid content of killer and non-killer cells is being analyzed to see if the biosynthesis of macromolecules changes when these cells differentiate into killer cells.